Sydenham's chorea, the neurological manifestation of rheumatic fever, is the most common acquired chorea of childhood. In this retrospective study, the authors aim to present the clinical and laboratory findings of 65 Sydenham's chorea patients, followed up in a clinic over less than 7 years. The mean age at the onset of the symptoms was 11.7 +/- 2.6 years (range, 6-17 years). Of the patients, 63% were female and 37% were male (male/female: 1.7/1). Chorea was generalized in 78.5% of the patients, right hemichorea in 12.3%, and left hemichorea 9.2%. There was a history of rheumatic fever in 30.8% of the patients. Echocardiographic study showed cardiac valve involvement in 70.5% of 61 patients. Brain magnetic resonance imaging, which was performed on only 18 patients, was evaluated as normal in all. Electroencephalography was also performed on only 18 patients and showed abnormal waves in 50% of them. Pimozide was mostly the first choice of drug therapy. Nevertheless, drug therapy was not needed in 18.5% of the patients. The recovery period of the first attack of the chorea was 1 to 6 months in 51.7% of the patients. The recurrence rate was 37.9%. In conclusion, Sydenham's chorea is still an important health problem in Turkey with respect to its morbidity.

The present study suggests that underlying mechanisms common to both macrosomic infants of nondiabetic mothers and IDMs lead to less cardiac alterations in the macrosomic infants of nondiabetic mothers than in IDMs.

This study presents clinical and laboratory findings and outcome of infants with intracranial hemorrhage (ICH) due to vitamin K deficiency after the newborn period, and evaluates vitamin K prophylaxis. The hospital records of 19 infants with a diagnosis of ICH due to vitamin K deficiency after the newborn period, seen in our clinic in less than 4 years, were retrospectively evaluated. The mean age at onset of the symptoms was 49 +/- 18 days. The most frequent presenting complaints were convulsion (58%), vomiting (47%), and irritability (47%). The most frequent examination findings were coma (74%), fontanel bulging (68%), and absence of pupil reaction (42%). The localizations of the ICHs were as follows: parenchymal (47%), subarachnoid (47%), subdural (42%), and intraventricular (26%). Four patients had used antibiotics and 1 patient had suffered diarrhea before the onset of the symptoms. One patient had a mild hepatic dysfunction that resolved spontaneously in a few weeks and its cause was not found. Mortality was observed in 6 (32%) patients. Ten patients were followed up for a mean period of 26.9 +/- 22.6 months. The follow-up findings were developmental delay (40%), microcephaly (30%), epilepsy (30%), blindness (20%), strabismus (20%), spastic tetraparesis (10%), spastic hemiparesis (10%), growth retardation (10%), and hydrocephaly (10%). Three (30%) patients remained neurologically normal. Vitamin K deficiency leads to death and neurological defects. Vitamin K prophylaxis at birth is therefore a priority. In this series, hepatic dysfunction had been detected in only 1 patient. The authors speculate that additional vitamin K to breast-fed infants with liver problem, antibiotic use, diarrhea, etc., should be considered.

A transient form of hypertrophic cardiomyopathy has been previously described in infants of diabetic mothers. When it occurs, it is generally benign. The purpose of our study was to establish the extent of injury to the cardiomyocytes in symptomatic and asymptomatic patients with and without hypertrophic cardiomyopathy.Thus, we compared 35 consecutive patients to 20 healthy controls, establishing the significance, if any, of differences in cardiac troponin-I and creatine kinase, including its MB-fraction, and seeking to establish the value of these parameters in the diagnosis of cardiac injury. We also determined to levels of glucose and insulin in the serum, and took note of electrocardiographic and echocardiographic investigations. Values were determined at the 1st and 7th days after admission in the patients, while parameters were measured in the control group only on the first day.We found that the levels of cardiac troponin-I in the serum, known to be a marker for cardiac injury, were significantly elevated in symptomatic patients with life-threatening respiratory or haemodynamic distress. We speculate that transient ventricular hypertrophy is neither the cause nor the consequence of damage to the cardiomyocytes. It would be interesting, nonetheless, to determine the relationship, if any, between cardiomyocytic damage and clinical outcome.